Introduction: Acute kidney injury is a major cause of excess hospitalizations during heat waves. The etiology of this acute kidney injury is likely contributed to by renal ischemia-reperfusion (IR) injury. Renal IR injury results in damage to the renal tubules and a subsequent impairment in sodium reabsorption. Fractional excretion of sodium is often used as an indirect marker of damage to the renal tubules and increases of gt;1% reflect ischemic acute kidney injury. Mechanistic studies, which are limited to rodent IR models, have reported that impairments in sodium reabsorption following ischemic acute kidney injury are mediated by a reduction in active transporters for sodium reabsorption in the renal tubules. However, similar in vivo studies are not possible in humans. The eccrine sweat glands have been proposed as a model of the nephrons given the anatomical and physiological similarities (e.g., sodium reabsorption).
Purpose: Test the hypothesis that sweat sodium concentrations are elevated following IR injury during passive heat stress.
Methods: Fifteen healthy adults (10 women; age: 25±3 y; body mass index: 23.7±3.5 kg·m-2) completed a cross-body design experiment consisting of ~160 min of passive heat stress (core body temperature: +1.5±0.2°C) utilizing a suit perfused with 50°C water. At 60 min of whole-body heating, one upper arm (randomized) was occluded (220 mmHg) for 20 min followed by reperfusion. Sweat was collected from the ventral aspect of each forearm via an absorbent patch (~77 cm2) pre- and post-IR for 24±4 and 30±6 min, respectively. Sweat sodium concentration (mmol·L-1) was measured in duplicate via electrolyte analyzer (EasyLyte® Plus). Local sweat rate was measured on the distal aspect of the dorsal forearm continuously via hygrometry (mL·min-1·cm-2). Comparisons were made between the experimental (IR) and control arms. Data are reported as mean±SD.
Results: Local sweat rate increased during whole-body passive heating (plt;0.001) and was not different between the experimental and control arms at any timepoint except during ischemia (0.45±0.53 vs.1.31±0.43 mL·min-1·cm-2, respectively; plt;0.001). Sweat sodium concentration did not change from pre- to post-IR in the control arm (pre: 54.9±32.2 mmol·L-1 and post: 58.7±25.6 mmol·L-1; p=0.99), but increased from pre- to post-IR in the experimental arm (pre: 48.4±23.3 mmol·L-1 and post: 63.8±30.9 mmol·L-1; p=0.02). Furthermore, the change from pre-IR in sweat sodium concentration was different between experimental and control arms post-IR (+12.5±14.70 mmol·L-1 versus -0.3±20.5 mmol·L-1, respectively; p=0.05).
Conclusion: In support of our hypothesis, sweat sodium concentration was elevated following IR injury and does not appear to be mediated by alterations in sweat rate. These observations are in-line with rodent renal IR models demonstrating impaired sodium reabsorption. While these findings appear to support the use of eccrine sweat glands as a model, further testing is required to verify its use to understand impaired sodium handling following IR injury in humans.
